Intact proactive motor inhibition after unilateral prefrontal cortex or basal ganglia lesions

Matthias Liebrand, Anne Kristin Solbakk, Ingrid Funderud, Macià Buades-Rotger, Robert T. Knight, Ulrike M. Krämer*

*Corresponding author for this work
3 Citations (Scopus)

Abstract

Previous research provided evidence for the critical importance of the PFC and BG for reactive motor inhibition, that is, when actions are cancelled in response to external signals. Less is known about the role of the PFC and BG in proactive motor inhibition, referring to preparation for an upcoming stop signal. In this study, patients with unilateral lesions to the BG or lateral PFC performed in a cued go/no-go task, whereas their EEG was recorded. The paradigm called for cue-based preparation for upcoming, lateralized no-go signals. Based on previous findings, we focused on EEG indices of cognitive control (prefrontal beta), motor preparation (sensorimotor mu/beta, contingent negative variation [CNV]), and preparatory attention (occip-ital alpha, CNV). On a behavioral level, no differences between patients and control s were found, suggesting an intact ability to proactively prepare for motor inhibition. Patients showed an altered preparatory CNV effect, but no other differences in electrophysiological activity related to proactive and reactive motor inhibition. Our results suggest a context-dependent role of BG and PFC structures in motor inhibition, being critical in reactive, unpredictable contexts, but less so in situations where one can prepare for stopping on a short timescale.

Original languageEnglish
JournalJournal of Cognitive Neuroscience
Volume33
Issue number9
Pages (from-to)1862-1879
Number of pages18
ISSN0898-929X
DOIs
Publication statusPublished - 01.08.2021

Funding

We are very thankful to all patients and control participants for participating, to Susanne Schellbach and Melanie Schildmann for data collection, and to Dr. Elinor Tzvi for help with data analysis. We are grateful to Dr. Torstein R. Meling for help with patient recruitment. U. M. K. was supported by the DFG (KR3691/8-1). R. T. K. was supported through the National Institute of Neurological Disorders (grant NS21135). A.-K. S. and I. F. were supported by a grant from the Research Council of Norway (project number 240389) and by the Research Council of Norway through its Centres of Excellence scheme (project number 262762 RITMO) and RITPART International Partnerships for RITMO Centre of Excellence (project number 274996). Ulrike M. Krämer, Deutsche Forschungsgemeinschaft (http://dx.doi.org/10.13039/501100001659), grant number: KR3691/8-1. Norges Forskningsråd (http://dx.doi.org /10.13039/501100005416), grant numbers: 240389, 262762 RITMO. National Institute of Neurological Disorders and Stroke (http://dx.doi.org/10.13039/100000065), grant number: NS21135.

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